Insulin is involved in the regulation of the blood glucose level. Insufficient release of insulin leads to various forms of diabetes.
The mechanisms of glucose-stimulated insulin secretion are the following: enhanced glucose metabolism increases intracellular ATP/ADP and closes ATP-dependent potassium (KATP) channels. At the same time, membrane depolarisation occurs, which induces opening of voltage-dependent calcium channels to increase the free cytosolic calcium ion concentration and stimulates insulin secretion (KATP-dependent pathway).
HIT-T15 cells are used because they exhibit a relatively high responsiveness to glucose.
Exposure duration: continuous for 15 min
Exposure duration: continuous for 10 min
immediately after flow cytometric analysis
|Setup||*acrylic CO2 incubator installed in the inner gap of the core. Cells were incubated in 0.4 mL KRBB (0) or Herpes buffered KRBB containing 0.2% BSA and 200 mg/dL glucose|
|Additional info||*information obtained from the reference article.|
The results showed that exposure to extremely low frequency magnetic field (5 mT) decreased glucose-stimulated insulin secretion from HIT-T15 cells. In absence of glucose stimulation or under exposure to lower magnetic flux density (less than 1 mT), insulin secretion was not changed.
Cellular mechanistic analysis revealed that irradiation to extremely low frequency magnetic field prevented the rises in cellular ATP/ADP, membrane depolarization, and cytosolic free calcium ion concentration. The glucose-induced upregulation of insulin mRNA expression was also attenuated by exposure to extreme low frequency magnetic field, although cell viability was not impaired.
The authors suggested that the findings demonstrate the potential of exposure to extremely low frequency magnetic field for clinical use as a novel inhibitory method of excessive insulin secretion in treatment of type 2 diabetes. (Remarks of the evaluator: At first there is an increased insulin production in type 2 diabetes due to the decreased responsiveness of the cells to insulin.)